The Inhibitory Effects of Sevoflurane on Angiotensin II- Induced, p44/42 Mitogen-Activated Protein Kinase-Mediated Contraction of Rat Aortic Smooth Muscle

Abstract

The present study demonstrates that sevoflurane can dose-dependently inhibit both angiotensin II (Ang II)-induced contraction and p44/42 MAPK phosphorylation of rat aortic smooth muscle. These data suggest that sevoflurane-produced inhibition of Ang II-induced vasoconstriction is, at least in part, caused by depression of the p44/42 MAPK-mediated signaling pathway.

Differential effects on the mesenteric microcirculatory response to vasopressin and phenylephrine after cardiopulmonary bypass

“…Isoflurane and sevoflurane have been associated with inhibition of ERK1/ 2-mediated vascular smooth muscle contraction. 19,20 The limitations of our study include the operative technique, the pharmacologic conditions, and the timing of vessel harvest. First, our CPB protocol was under normothermia, whereas many clinical cardiac surgical procedures involve CPB with some degree of hypothermia.…”

Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat

“…The strips were then exposed to Ang II for 4 min, which was based upon our previous investigations [15,19,20], and then rapidly frozen on dry ice. Seven additional aortas of each strain without Ang II and sevoflurane treatment served as a baseline control.…”

Prolonged attenuation of acetylcholine‐induced phosphorylation of extracellular signal‐regulated kinase 1/2 following sevoflurane exposure

“…As previously shown, volatile anaesthetics can affect lipid bilayer fluidity, which could interfere with receptor function directly or via membrane‐associated processes such as G protein activation or effector regulation and allosteric effects on receptor proteins. It could also be possible that cytoplasmic signalling components, such as the MAPK cascade, are affected, although others have described that intracellular pathways that downstream the G protein are not affected by volatile anaesthetics . We therefore believe that the mechanisms behind the attenuation of acetylchline‐induced phosphorylation of ERK 1/2 are located somewhere in the vincinity of the metabotropic G protein‐coupled mAChR, either by acting on agonist binding, by allosteric receptor modulation or by interfering with G protein activation and second messenger amplification of the signal.…”